Spontaneous coronary artery dissection is a rare and underdiagnosed cause of acute coronary syndrome, primarily affecting women. The occurrence of spontaneous coronary artery dissection in the context of the absence of traditional atherosclerotic risk factors raises questions about the role of physical exertion or other stressors as potential triggers. Early recognition through clinical assessment and imaging is essential, as the therapeutic approach for spontaneous coronary artery dissection differs significantly from the treatment of traditional atherosclerotic acute coronary syndrome. Conservative management is often preferred for hemodynamically stable patients because interventional procedures have increased prevalence of complications in these patients. This case report highlights an uncommon presentation of spontaneous coronary artery dissection in a 28-year-old man who presented with non-ST-elevation myocardial infarction following physical exertion. The diagnosis of spontaneous coronary artery dissection was confirmed via coronary angiography, revealing the classic findings of dissection without significant atherosclerosis. Management was conservative, as the patient was hemodynamically stable, with close monitoring and medical therapy, including antiplatelet agents and beta-blockers. This case challenges the prevailing gender assumptions associated with spontaneous coronary artery dissection and highlights the need for increased awareness of spontaneous coronary artery dissection in males. Additionally, it suggests the potential role of physical stressors in precipitating spontaneous coronary artery dissection. Further research into the pathophysiology of spontaneous coronary artery dissection in different populations is warranted.

Objectives: Permanent pacemakers are widely used to manage symptomatic bradyarrhythmias and conduction disorders; however, their impact on hospitalization outcomes, such as length of stay, in patients with acute decompensated diastolic heart failure remains unclear. This study aimed to assess whether prior pacemaker implantation independently affects hospital length of stay using data from the 2018-2019 National Inpatient Sample database. Methods: A total of 14,523 adult patients hospitalized with acute diastolic heart failure were identified, including 855 with a history of pacemaker implantation. Propensity score matching was conducted to adjust for baseline differences, and competing risks regression was performed to account for the competing risk of in-hospital mortality. Results: Before matching, pacemaker recipients were older and had a higher burden of comorbidities; unadjusted analysis showed a modest but statistically significant association with shorter length of stay (sHR = 1.075; 95% CI: 1.010-1.144; P = 0.023). After matching, this association was attenuated and no longer significant (sHR = 1.081; 95% CI: 0.992-1.178; P = 0.077). Comorbid conditions, particularly chronic kidney disease, liver disease, and pulmonary hypertension, were stronger predictors of prolonged hospitalization. Conclusions: These findings suggest that pacemaker status alone does not independently affect the length of stay in patients hospitalized with acute diastolic heart failure, highlighting the importance of managing comorbidities to potentially reduce hospital length of stay in this vulnerable population, although further studies are warranted to confirm these observations.

Cardiac amyloidosis is an infiltrative cardiomyopathy caused by extracellular deposition of misfolded proteins, most commonly immunoglobulin light chains (AL) or transthyretin (ATTR), with rarer forms occurring less frequently. AL amyloidosis arises from plasma cell-derived light chains and typically follows an aggressive clinical course, whereas ATTR amyloidosis results from misfolded wild-type or variant transthyretin and progresses more indolently. Extracellular vesicles (EVs) have recently been recognized as mediators of amyloid propagation, inflammation, and myocardial remodeling, particularly at later stages of disease. Despite growing evidence, no comprehensive reviews have focused on this relationship. We conducted a structured narrative review (PubMed and Scopus, 2020–2025) following Preferred Reporting Items for Systematic reviews and Meta-Analyses extension for Scoping Reviews (PRISMA-ScR) guidelines to synthesize emerging data. EVs act as scaffolds for transthyretin and serum amyloid A aggregation and carry disease-specific protein and RNA cargo detectable in blood and urine. Experimental models also demonstrate EV-mediated transport of serum amyloid A under conditions of cardiac stress, representing a reactive amyloidogenic pathway rather than a common cause of human cardiac amyloidosis. Preclinical studies show regenerative and anti-fibrotic effects of stem-cell-derived EVs, and early clinical trials demonstrate the feasibility of EV-based cardiac therapy. While methodological and translational challenges persist, EVs represent promising diagnostic and therapeutic tools that could transform the precision management of cardiac amyloidosis.